p38 MAPK signaling is a key mediator for low-intensity pulsed ultrasound (LIPUS) in cultured human omental adipose-derived mesenchymal stem cells.

Visceral obesity is an independent risk factor for cardiovascular disorders and lacks effective, non-drug based clinical therapy. The use of low-intensity pulsed ultrasound (LIPUS) to treat chronic pain and bone fracture is well-known, but its application for visceral obesity treatment has not been studied. Here, we evaluated the therapeutic potential of LIPUS by studying its effects, at varying doses, on human omental adipose-derived mesenchymal stem cells (hAMSCs). LIPUS stimulation was applied for 1 min at intensities between 70 and 210 mW/cm2. Cell viability was measured using the Cell Counting Kit-8 assay. Cell apoptosis was quantified by flow cytometry and immunoblotting of apoptosis marker proteins. We found that a high dose of LIPUS (210 mW/cm2) promoted apoptosis in hAMSCs, while a low dose (70 mW/cm2) increased hAMSC viability. Phosphorylation of p38, a mitogen-activated protein kinase (MAPK), increased with high dose LIPUS treatment, but markedly decreased with a low dose. Inhibition of p38 phosphorylation by SB203580, an inhibitor of p38 MAPK activity, rescued the apoptotic effects of high dose LIPUS. Our results showed the dose-dependent, opposing effects of LIPUS on hAMSCs and suggested that p38 plays a key role in mediating the effects of LIPUS on hAMSCs.